INHIBITION OF G1 CYCLIN ACTIVITY BY THE RAS CAMP PATHWAY IN YEAST/

IN the yeast Saccharomyces cerevisiae, commitment to cell division (St art) requires growth to a critical cell size(1-3). The G1 cyclins Cln1 , Cln2 and Cln3 activate the Cdc28 protein kinase and are rate-limitin g activators of Start(4-6). When glucose is added to cells growing in a poor carbon source, the critical cell size required for Start is res et from a small to a large size(2,3,7). In yeast, glucose acts through Ras proteins to stimulate adenylyl cyclase, activating the three cycl ic AMP-dependent protein kinases Tpk1, Tpk2 and Tpk3 (refs 8, 9). We f ind that stimulation of the Ras/cAMP pathway represses expression of C LN1, CLN2 and co-regulated genes, inhibiting Start. This helps explain the increase in critical size when cells are shifted from poor to ric h medium. This connection between the molecules controlling growth (Ra s/cAMP) and those controlling division (cyclins) helps explain how div ision is co-ordinated with growth.